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Effect of acetylcholine receptors on the pain-related electrical activities in the hippocampal CA3 region of morphine-addicted rats.

Li GZ, Liu ZH, Wei X, Zhao P, Yang CX, Xu MY - Iran J Basic Med Sci (2015)

Bottom Line: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN.The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect.Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Liaocheng People's Hospital, 67 Dongchang Xi Road, Liaocheng 252000, China.

ABSTRACT

Objectives: To determine the effect of acetylcholine (ACh), pilocarpine, and atropine on pain evoked responses of pain excited neurons (PEN) and pain inhibited neurons (PIN) in hippocampal CA3 region of morphine addicted rats.

Materials and methods: Female Wistar rats, weighing between 230-260 g were used in this study. Morphine addicted rats were generated by subcutaneous injection of increasing concentrations of morphine hydrochloride for six days. Trains of electrical impulses applied to the sciatic nerve were used as noxious stimulation and the evoked electrical activities of PEN or PIN in hippocampal CA3 area were recorded using extracellular electrophysiological recording techniques in hippocampal slices. The effect of acetylcholine receptor stimulation by ACh, the muscarinic agonist pilocarpine, and the muscarinic antagonist atropine on the pain evoked responses of pain related electrical activities was analyzed in hippocampal CA3 area of morphine addicted rats.

Results: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN. The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect. The peak activity of cholinergic modulators was 2 to 4 min later in morphine addicted rats compared to peak activity previously observed in normal rats.

Conclusion: ACh dependent modulation of noxious stimulation exists in hippocampal CA3 area of morphine addicted rats. Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

No MeSH data available.


Influence of intra-CA3 injection of different substances on the NIV (A) and ID (B) of PIN in the CA3 of morphine-addicted rats ▄, injection of substance; X, before injection; 0, 2,…, 30, time after injection (min); values are presented as means±SEM. *P <0.05, **P<0.01, #P<0.05, ##P<0.01, ΔP<0.05, ΔΔP<0.01, when compared with the saline control group
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Figure 5: Influence of intra-CA3 injection of different substances on the NIV (A) and ID (B) of PIN in the CA3 of morphine-addicted rats ▄, injection of substance; X, before injection; 0, 2,…, 30, time after injection (min); values are presented as means±SEM. *P <0.05, **P<0.01, #P<0.05, ##P<0.01, ΔP<0.05, ΔΔP<0.01, when compared with the saline control group

Mentions: The average NIV of PINs was −4.41±0.78 Hz, and the average ID of PINs was 0.31±0.06 sec. Immediately after injection of ACh, the average NIV began to increase and ID began to shorten (Figure 3B). These changes reached a peak value at 10 min after injection; with the average NIV at −0.91±0.27 Hz (F= 392.202, P < 0.0001) and the ID decreased to 0.1±0.02 sec (F= 257.19, P<0.0001). The average NIV (F= 41.187, P<0.0001) showed significant differences compared to values before injection between the time points of 0-18 min after injection. Between 0-20 min after injection, the ID (F= 12.832, P= 0.006) of PINs showed significant differences compared to values before injection. Between the time points of 2-16 min after administration, the NIV, and between the time points of 2-18 min after administration, ID showed significant changes (P<0.05 or P<0.01) compared with those of the control group (Figure 5).


Effect of acetylcholine receptors on the pain-related electrical activities in the hippocampal CA3 region of morphine-addicted rats.

Li GZ, Liu ZH, Wei X, Zhao P, Yang CX, Xu MY - Iran J Basic Med Sci (2015)

Influence of intra-CA3 injection of different substances on the NIV (A) and ID (B) of PIN in the CA3 of morphine-addicted rats ▄, injection of substance; X, before injection; 0, 2,…, 30, time after injection (min); values are presented as means±SEM. *P <0.05, **P<0.01, #P<0.05, ##P<0.01, ΔP<0.05, ΔΔP<0.01, when compared with the saline control group
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556759&req=5

Figure 5: Influence of intra-CA3 injection of different substances on the NIV (A) and ID (B) of PIN in the CA3 of morphine-addicted rats ▄, injection of substance; X, before injection; 0, 2,…, 30, time after injection (min); values are presented as means±SEM. *P <0.05, **P<0.01, #P<0.05, ##P<0.01, ΔP<0.05, ΔΔP<0.01, when compared with the saline control group
Mentions: The average NIV of PINs was −4.41±0.78 Hz, and the average ID of PINs was 0.31±0.06 sec. Immediately after injection of ACh, the average NIV began to increase and ID began to shorten (Figure 3B). These changes reached a peak value at 10 min after injection; with the average NIV at −0.91±0.27 Hz (F= 392.202, P < 0.0001) and the ID decreased to 0.1±0.02 sec (F= 257.19, P<0.0001). The average NIV (F= 41.187, P<0.0001) showed significant differences compared to values before injection between the time points of 0-18 min after injection. Between 0-20 min after injection, the ID (F= 12.832, P= 0.006) of PINs showed significant differences compared to values before injection. Between the time points of 2-16 min after administration, the NIV, and between the time points of 2-18 min after administration, ID showed significant changes (P<0.05 or P<0.01) compared with those of the control group (Figure 5).

Bottom Line: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN.The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect.Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Liaocheng People's Hospital, 67 Dongchang Xi Road, Liaocheng 252000, China.

ABSTRACT

Objectives: To determine the effect of acetylcholine (ACh), pilocarpine, and atropine on pain evoked responses of pain excited neurons (PEN) and pain inhibited neurons (PIN) in hippocampal CA3 region of morphine addicted rats.

Materials and methods: Female Wistar rats, weighing between 230-260 g were used in this study. Morphine addicted rats were generated by subcutaneous injection of increasing concentrations of morphine hydrochloride for six days. Trains of electrical impulses applied to the sciatic nerve were used as noxious stimulation and the evoked electrical activities of PEN or PIN in hippocampal CA3 area were recorded using extracellular electrophysiological recording techniques in hippocampal slices. The effect of acetylcholine receptor stimulation by ACh, the muscarinic agonist pilocarpine, and the muscarinic antagonist atropine on the pain evoked responses of pain related electrical activities was analyzed in hippocampal CA3 area of morphine addicted rats.

Results: Intra-CA3 microinjection of ACh (2 μg/1 μl) or pilocarpine (2 μg/1 μl) decreased the discharge frequency and prolonged the firing latency of PEN, but increased the discharge frequency and shortened the firing inhibitory duration (ID) of PIN. The intra-CA3 administration of atropine (0.5 μg/1 μl) produced opposite effect. The peak activity of cholinergic modulators was 2 to 4 min later in morphine addicted rats compared to peak activity previously observed in normal rats.

Conclusion: ACh dependent modulation of noxious stimulation exists in hippocampal CA3 area of morphine addicted rats. Morphine treatment may shift the sensitivity of pain related neurons towards a delayed response to muscarinergic neurotransmission in hippocampal CA3 region.

No MeSH data available.